In vitro damage to rat intestine by enteropathogenic E.coli as revealed by release of β-glucosidases

Abstract

Enteropathogenic E. Coli (EPEC) causes persistent diarrhea, resulting in high mortality and morbidity among infants. EPEC forms micro colonies on intestinal epithelial cells and causes a characteristic ‘attaching and effacing’ (A/E) epithelial lesion, which destructs microvillus and the intimate attachment of bacteria to form a pedestal-like structure on the surface of epithelial cells. In present in vitro study, effect of EPEC infection on damage caused to functional integrity of brush border was studied by monitoring ²-glucosidase activity, which is essential for dietary carbohydrate digestion. There was a release of glucoamylase, sucrase and maltase from brush border ileal region. Both virulent and attenuated strains of EPEC were able to do so indicating that ability of EPEC might lie in an unknown chromosomal locus. In a short incubation time, a net synthesis of b-glucosidase during infection to replenish loss was observed. This might represent host response in early phase of EPEC infection.